Fig. 2.

KDO25 promotes regression of TAA-induced liver fibrosis.

(A) C57BL/6 mice were treated with TAA for 6 weeks followed by 2 weeks of TAA and vehicle or TAA and KD025 co-administration. Histochemical staining and Aperio quantification of (B) SR, (C) SMA, and (D) pan-keratin (CK-WSS) in liver sections were undertaken (n = 4–6 animals/group). Representative images are shown. (E) Expression of col-1a mRNA in whole liver was determined by qRT-PCR and normalised to HPRT mRNA levels (n = 6–9 animals/group; combined from 2 independent experiments). (F) Absolute number of monocytes, eosinophils, and granulocytes was determined by flow cytometry (n = 10 animals/group; combined from 2 independent experiments). Representative images, and data are presented as mean ± SEM. ∗p <0.05, ∗∗p <0.01 Mann–Whitney U test. qRT-PCR, quantitative real-time PCR; SMA, smooth muscle actin; SR, Sirius red; TAA, thioacetamide; WSS, wide spectrum screening.